1/268. Acquired and isolated asymmetrical palatal palsy.Benign acquired and isolated asymmetrical palatal palsy is a rare condition in childhood. We report on three cases. Typical features include: sudden onset, abnormality of the palatal components of speech (rhinolalia), nasal escape of fluids from the ipsilateral nostril. It is supposed to be caused by viral infection, but attempts at viral isolation were unsuccessful. Complete spontaneous recovery is usual, taking a few weeks. Our paper seems to be the first report of magnetic resonance imaging of the brain in this condition. It did not disclose any abnormalities in the 2 cases in which it was performed.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
2/268. MR and CT imaging in the Dyke-Davidoff-Masson syndrome. Report of three cases and contribution to pathogenesis and differential diagnosis.Cerebral hemiatrophy or Dyke-Davidoff-Masson syndrome is a condition characterized by seizures, facial asymmetry, contralateral hemiplegia or hemiparesis, and mental retardation. These findings are due to cerebral injury that may occur early in life or in utero. The radiological features are unilateral loss of cerebral volume and associated compensatory bone alterations in the calvarium, like thickening, hyperpneumatization of the paranasal sinuses and mastoid cells and elevation of the petrous ridge. The authors describe three cases. Classical findings of the syndrome are present in variable degrees according to the extent of the brain injury. Pathogenesis is commented.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
3/268. A case of the subacute brainstem encephalitis.A case of brainstem encephalitis of undetermined etiology is reported in 66-year-old woman who had a sudden onset of illness with left abducens palsy, nystagmus and ataxia. The symptoms progressed to complete paralysis of eye movements, dysphagia and left hemiparesis with generalized hyperreflexia. Examination of CSF, CT scan and MRI of the brain were normal. The patient died 4 months after onset of disease. Neuropathologic study disclosed in the brainstem numerous perivascular and nodular inflammatory cell infiltrations composed predominantly of lymphocytes T and B. Most intensive inflammation concerned midbrain and pontine tegmentum and to a lesser degree medulla oblongata, pontine nuclei and cerebellar nuclei. basal ganglia, cerebral and cerebellar cortex were unaffected. Neuropathological finding was reminiscent of brainstem encephalitides related to viral infection or to paraneoplastic syndrome. However, HSV-1, EBV, and CMV antigens were not detected by immunohistochemistry, as well as evidences of malignancy were not present in this case.- - - - - - - - - - ranking = 9keywords = brain (Clic here for more details about this article) |
4/268. On some neurobiological and cultural-anthropological aspects of the contralateral-neglect syndrome.Contralateral neglect is a frequent clinical syndrome which can be provoked by lesions in several brain areas (primarily inferior parietal and frontal) and includes symptoms of motor and perceptual negligence of both real and imaginative contralateral hemi-space. Attentional and representative theories attempting to explain neglect are presently the most popular. This paper analyzes two cases of neglect patients. Paying attention especially to their reading defects, a possible role of the persons with contralateral neglect is proposed in the development of script. Other neurobiological and cultural-anthropological questions arising from the analysis of these cases are also discussed.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
5/268. Localized scleroderma associated with progressing ischemic stroke.We present a 73 year-old Japanese woman with localized scleroderma involving the right side of the scalp accompanied by continuous tingling pain, who developed insidiously progressive left hemiparesis. In magnetic resonance imaging of the brain, an infarct first appeared in the watershed region of the right middle cerebral artery territory and subsequently extended to deep white matter accompanied by scattered hemorrhages. Focal stenosis in the M2 portion of the right middle cerebral artery was revealed on magnetic resonance angiography, and the distal vessels were only shown faintly. A biopsy specimen from the sclerotic scalp lesion showed obvious thickening of vessel walls and mild mononuclear cell infiltration. We believe that the progressing ischemic stroke was caused by hemodynamic disturbances from localized sclerotic obstruction of the middle cerebral artery, with an autoimmune pathogenesis.- - - - - - - - - - ranking = 1keywords = brain (Clic here for more details about this article) |
6/268. A new CACNA1A gene mutation in acetazolamide-responsive familial hemiplegic migraine and ataxia.OBJECTIVE: To search for mutations in the calcium channel gene CACNA1A and to study the genotype-phenotype correlation in a family with a severe familial hemiplegic migraine (FHM) phenotype and a slowly progressive cerebellar ataxia. BACKGROUND: CACNA1A gene mutations on chromosome 19 are involved in approximately 50% of FHM families. The association of FHM and cerebellar ataxia has been reported in a small number of FHM families, all linked to chromosome 19. methods: The proband, in addition to typical hemiplegic migraine attacks, experienced severe episodes during which hemiplegia was associated with acutely altered consciousness and fever lasting several days. She, as well as her affected sister, developed a permanent, late-onset cerebellar ataxia and cerebellar atrophy evident on MRI. Linkage analysis was performed and the whole CACNA1A gene, 47 exon-intron boundaries, was analyzed by double gradient-denaturing gradient gel electrophoresis (DG-DGGE). RESULTS: Genetic studies suggested linkage to chromosome 19p13, and DG-DGGE analysis detected a heteroduplex fragment in exon 13 of the CACNA1A gene. By direct sequencing, a G-to-A substitution resulting in an arginine to glutamine change at codon 583 in the second putative voltage sensor domain of the channel alpha1A-subunit, was identified, possibly representing the disease-causing mutation. The proband and her affected sister were treated with acetazolamide, reporting freedom from new FHM attacks but no benefit in the progression of ataxia. CONCLUSIONS: The combination of episodic dysfunction and permanent deficit could depend on the variety of functions of calcium channels and their distribution in the nervous system.- - - - - - - - - - ranking = 0.18965650751165keywords = nervous system (Clic here for more details about this article) |
7/268. Aggravation of brainstem symptoms caused by a large superior cerebellar artery aneurysm after embolization by Guglielmi detachable coils--case report.An 81-year-old male presented with right oculomotor nerve paresis and left hemiparesis caused by a mass effect of a large superior cerebellar artery aneurysm. Endovascular treatment was performed using Guglielmi detachable coils. The patient subsequently suffered aggravation of the mass effect 3 weeks after the embolization. Bilateral vertebral artery occlusion was performed, which decreased the cerebral edema surrounding the aneurysm, but his neurological symptoms did not improve. Parent artery occlusion is recommended as the first choice of treatment for an unclippable large or giant aneurysm causing a mass effect on the brainstem.- - - - - - - - - - ranking = 5keywords = brain (Clic here for more details about this article) |
8/268. Weber's syndrome secondary to subarachnoid hemorrhage.BACKGROUND: Since a large intracranial hemorrhage is a space-occupying mass, it may cause the brain to shift, resulting in neurologic deficits both at the location of the bleeding and at a site distal to the hemorrhage. A parietal lobe hemorrhage may push the brain downward, causing the uncus of the temporal lobe to herniate through the tentorial notch, compressing the midbrain. The signs of parietal lobe damage, uncal herniation, and several midbrain syndromes that effect ocular motility are discussed. CASE REPORT: A 66-year-old Hispanic man came to us with a history of a subarachnoid hemorrhage that involved the right parietal lobe. Several signs of damage to both the right parietal lobe and midbrain were evident, including an ipsilateral third nerve paresis with contralateral hemiplegia, Weber's syndrome. CONCLUSION: A patient who survives a subarachnoid hemorrhage may demonstrate permanent residual neurologic deficits subsequent to the acute event. The presentation is particularly complex when the hemorrhage is large and damage occurs at multiple locations. Damage at the level of the midbrain is evident when the findings include Weber's syndrome, which is one of several syndromes that involves the oculomotor nerve.- - - - - - - - - - ranking = 6keywords = brain (Clic here for more details about this article) |
9/268. hemiplegia hypoglycaemia syndrome.We report the case of a 83-year-old man who presented to the emergency department with hypoglycaemia resembling a cerebrovascular accident. Hypoglycaemic hemiparesis is an under-recognized manifestation of hypoglycaemia. If not recognized and treated promptly, hypoglycaemia may cause irreversible central nervous system injury; it rarely results in death. It is imperative that emergency physicians consider hypoglycaemia in all patients with coma in spite of focal neurological deficit even when the findings seem to be explained initially by other aetiologies.- - - - - - - - - - ranking = 0.74745039976161keywords = central nervous system, nervous system (Clic here for more details about this article) |
10/268. Bilateral chronic subdural hematomas resulting in unilateral oculomotor nerve paresis and brain stem symptoms after operation--case report.An 85-year-old male presented with bilateral chronic subdural hematomas (CSDHs) resulting in unilateral oculomotor nerve paresis and brainstem symptoms immediately after removal of both hematomas in a single operation. Initial computed tomography on admission demonstrated marked thick bilateral hematomas buckling the brain parenchyma with a minimal midline shift. Almost simultaneous removal of the hematomas was performed with the left side was decompressed first with a time difference of at most 2 minutes. However, the patient developed right oculomotor nerve paresis, left hemiparesis, and consciousness disturbance after the operation. The relatively marked increase in pressure on the right side may have caused transient unilateral brain stem compression and herniation of unilateral medial temporal lobe during the short time between the right and left procedures. Another factor was the vulnerability of the oculomotor nerve resulting from posterior replacement of the brain stem and stretching of the oculomotor nerves as seen on sagittal magnetic resonance (MR) images. Axial MR images obtained at the same time demonstrated medial deflection of the distal oculomotor nerve after crossing the posterior cerebral artery, which indicates previous transient compression of the nerve and the brain stem. Gradual and symmetrical decompression without time lag is recommended for the treatment of huge bilateral CSDHs.- - - - - - - - - - ranking = 9keywords = brain (Clic here for more details about this article) |
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